人促甲状腺激素受体在缺乏内源性促甲状腺激素受体的人甲状腺癌细胞系中的表达：环磷酸腺苷介导的生长抑制作用

Expression of the human TSH receptor in a human thyroid carcinoma cell line that lacks an endogenous TSH receptor: growth inhibition by cAMP.

作者信息

Derwahl M, Kuemmel M, Goretzki P, Schatz H, Broecker M

机构信息

Laboratory of Experimental Endocrinology, Clinic of Internal Medicine, University of Bochum, Germany.

出版信息

Biochem Biophys Res Commun. 1993 Mar 31;191(3):1131-8. doi: 10.1006/bbrc.1993.1334.

DOI:10.1006/bbrc.1993.1334

PMID:8385451

Abstract

The role of TSH and its receptor in controlling growth of thyroid carcinomas is far from well understood. In order to study this subject further we established a new human thyroid carcinoma cell line. We transfected human thyroid carcinoma cells lacking an endogenous TSH receptor with the human TSH receptor cDNA. Transfected cells, designated HTC-TSHr, expressed the TSH receptor mRNA and synthesized a functional TSH receptor with a TSH binding affinity in the order of magnitude of normal thyroid cells. In response to TSH stimulation HTC-TSHr cells accumulated cAMP, indicating a functional TSH receptor-adenylate cyclase system. However, HTC-TSHr cells did not concentrate iodide and lacked thyroglobulin immunoreactivity, although they did express low amounts of thyroglobulin mRNA. Proliferation of HTC-TSHr cells was inhibited by dibutyryl-cAMP and forskolin and also by TSH via the re-expressed TSH receptor.

摘要

促甲状腺激素（TSH）及其受体在控制甲状腺癌生长中的作用远未被充分了解。为了进一步研究这个问题，我们建立了一种新的人甲状腺癌细胞系。我们用人类TSH受体cDNA转染缺乏内源性TSH受体的人甲状腺癌细胞。转染后的细胞，命名为HTC-TSHr，表达TSH受体mRNA，并合成了具有与正常甲状腺细胞数量级相当的TSH结合亲和力的功能性TSH受体。响应TSH刺激，HTC-TSHr细胞积累环磷酸腺苷（cAMP），表明存在功能性TSH受体-腺苷酸环化酶系统。然而，HTC-TSHr细胞不摄取碘，缺乏甲状腺球蛋白免疫反应性，尽管它们确实表达少量的甲状腺球蛋白mRNA。HTC-TSHr细胞的增殖受到二丁酰-cAMP和福斯可林的抑制，也受到通过重新表达的TSH受体的TSH的抑制。